BACKGROUND: Childhood obesity has become a major global health problem. Obesity is associated with major health problems, such as diabetes, hypertension, dyslipidemia, cardiovascular disease. Obesity is also considered a risk factor for Pseudotumor cerebri (PTC). The present study aimed to investigate the relationship between body mass index (BMI), and cerebrospinal fluid (CSF) pressure in patients with pseudotumor cerebri.
METHODS: A total of 48 children diagnosed with PTC, who were aged < 18 years and followed up in the pediatric clinic were included in the retrospective study. National BMI percentile curves were used for reference. We investigated statistically the relationship between BMI, clinical and laboratory results, and CSF pressure in patients.
RESULTS: Of total patients 27 were female (56.25%) and 21 were male (43.75%). With regard to the BMI percentile, 20 (41.67%) were overweight or obese. CSF pressure was higher in overweight and obese patients compared to children with BMI in normal ranges (p < 0.05). A statistically significant positive correlation was also observed between BMI and CSF pressure values and between monocyte and CSF values (p < 0.05).
CONCLUSIONS: The results of the present study indicate a direct relationship between CSF pressure and BMI in children with PTC. Appropriate diet, exercise, and medical treatment in overweight and obese children can make a significant contribution to the treatment of PTC. Additionally, a significant correlation was observed between CSF pressure and monocyte levels.

The principles of cerebrospinal fluid (CSF) production, circulation and outflow and regulation of fluid volumes and pressures in the normal brain are summarised. Abnormalities in these aspects in intracranial hypertension, ventriculomegaly and hydrocephalus are discussed. The brain parenchyma has a cellular framework with interstitial fluid (ISF) in the intervening spaces. Framework stress and interstitial fluid pressure (ISFP) combined provide the total stress which, after allowing for gravity, normally equals intracerebral pressure (ICP) with gradients of total stress too small to measure. Fluid pressure may differ from ICP in the parenchyma and collapsed subarachnoid spaces when the parenchyma presses against the meninges. Fluid pressure gradients determine fluid movements. In adults, restricting CSF outflow from subarachnoid spaces produces intracranial hypertension which, when CSF volumes change very little, is called idiopathic intracranial hypertension (iIH). Raised ICP in iIH is accompanied by increased venous sinus pressure, though which is cause and which effect is unclear. In infants with growing skulls, restriction in outflow leads to increased head and CSF volumes. In adults, ventriculomegaly can arise due to cerebral atrophy or, in hydrocephalus, to obstructions to intracranial CSF flow. In non-communicating hydrocephalus, flow through or out of the ventricles is somehow obstructed, whereas in communicating hydrocephalus, the obstruction is somewhere between the cisterna magna and cranial sites of outflow. When normal outflow routes are obstructed, continued CSF production in the ventricles may be partially balanced by outflow through the parenchyma via an oedematous periventricular layer and perivascular spaces. In adults, secondary hydrocephalus with raised ICP results from obvious obstructions to flow. By contrast, with the more subtly obstructed flow seen in normal pressure hydrocephalus (NPH), fluid pressure must be reduced elsewhere, e.g. in some subarachnoid spaces. In idiopathic NPH, where ventriculomegaly is accompanied by gait disturbance, dementia and/or urinary incontinence, the functional deficits can sometimes be reversed by shunting or third ventriculostomy. Parenchymal shrinkage is irreversible in late stage hydrocephalus with cellular framework loss but may not occur in early stages, whether by exclusion of fluid or otherwise. Further studies that are needed to explain the development of hydrocephalus are outlined.

UNASSIGNED: In-office use of the Trendelenburg position has been shown to be a beneficial clinical tool to help decipher if a CSF pressure/volume component is part of the underlying etiologic process for a patient\'s persistent headache. Utilizing the Trendelenburg position at home could potentially be an additional diagnostic tool for the treating headache physician.
UNASSIGNED: Our headache practice has been using at-home self-Trendelenburg for the past 2 years and will present the clinical scenarios in which it seems to be the most helpful utilizing a case series of patients. These include (1) in those who just had a lumbar puncture and call for worsening headaches and do not have an obvious orthostatic component; (2) in those who had a spinal epidural blood patch for a presumed CSF leak and state there was no improvement; (3) in those who are on daily preventive CSF volume-lowering medications and call in with worsening headaches; (4) in those with known CSF pressure-dependent headaches high or low but who are not on daily preventive CSF volume modulatory medications; (5) in those with a history of migraine or other primary headache disorder to see if a new type of headache is possibly from a CSF leak or an abnormal reset of CSF pressure to an elevated state; (6) in those with triggered only headaches like cough or exertional headache.
UNASSIGNED: Utilizing at-home self-Trendelenburg can provide valuable information for the treating headache physician on possible underlying headache etiology and can guide specific treatment strategies. Its simplicity and quick declaration of results are very patient pleasing.

BACKGROUND: Studies indicate that brain clearance via the glymphatic system is impaired in idiopathic normal pressure hydrocephalus (INPH). This has been suggested to result from reduced cerebrospinal fluid (CSF) turnover, which could be caused by a reduced CSF formation rate. The aim of this study was to determine the formation rate of CSF in a cohort of patients investigated for INPH and compare this to a historical control cohort.
METHODS: CSF formation rate was estimated in 135 (75 ± 6 years old, 64/71 men/women) patients undergoing investigation for INPH. A semiautomatic CSF infusion investigation (via lumbar puncture) was performed. CSF formation rate was assessed by downregulating and steadily maintaining CSF pressure at a zero level. During the last 10 min, the required outflow to maintain zero pressure, i.e., CSF formation rate, was continuously measured. The values were compared to those of a historical reference cohort from a study by Ekstedt in 1978.
RESULTS: Mean CSF formation rate was 0.45 ± 0.15 ml/min (N = 135), equivalent to 27 ± 9 ml/hour. There was no difference in the mean (p = 0.362) or variance (p = 0.498) of CSF formation rate between the subjects that were diagnosed as INPH (N = 86) and those who were not (N = 43). The CSF formation rate in INPH was statistically higher than in the reference cohort (0.46 ± 0.15 vs. 0.40 ± 0.08 ml/min, p = 0.005), but the small difference was probably not physiologically relevant. There was no correlation between CSF formation rate and baseline CSF pressure (r = 0.136, p = 0.115, N = 135) or age (-0.02, p = 0.803, N = 135).
CONCLUSIONS: The average CSF formation rate in INPH was not decreased compared to the healthy reference cohort, which does not support reduced CSF turnover. This emphasizes the need to further investigate the source and routes of the flow in the glymphatic system and the cause of the suggested impaired glymphatic clearance in INPH.

BACKGROUND: An increase in epidural pressure around the stenosis has been observed in patients with lumbar spinal stenosis (LSS) with positive signs of sedimentation or redundant nerve roots. Further analysis of the pressure conditions in the stenotic area would be of great interest. We hypothesized that it would be possible to determine the physiological parameters of the epidural pulse wave and its course in pathological stenosis as a basis for objective identification of LSS based on pressure using a new measuring method with continuous spatial and temporal resolution.
METHODS: We performed a single-case proof-of-principle in vivo animal trial and used a newly developed hybrid pressure-measurement probe with a fiber-tip Fabry-Pérot interferometer and several fiber Bragg gratings (FBG).
RESULTS: With reproducible precision, we determined the mean epidural pressure to be 7.5 mmHg and the peak-to-peak value to be 4-5 mmHg. When analyzing the pressure measured by an FBG array, both the heart and respiratory rates can be precisely determined. This study was the first to measure the pulse wave velocity of the cerebrospinal fluid pressure wave as 0.97 m/s using the newly developed pressure probe. A simulated LSS was detected in real time and located exactly.
CONCLUSIONS: The developed fiber-optic pressure sensor probe enables a new objective measurement of epidural pressure. We confirmed our hypothesis that physiological parameters of the epidural pulse wave can be determined and that it is possible to identify an LSS.

Chiari type 1 malformation is a neurological disorder characterized by an obstruction of the cerebrospinal fluid (CSF) circulation between the brain (intracranial) and spinal cord (spinal) compartments. Actions such as coughing might evoke spinal cord complications in patients with Chiari type 1 malformation, but the underlying mechanisms are not well understood. More insight into the impact of the obstruction on local and overall CSF dynamics can help reveal these mechanisms. Therefore, our previously developed computational fluid dynamics framework was used to establish a subject-specific model of the intracranial and upper spinal CSF space of a healthy control. In this model, we emulated a single cough and introduced porous zones to model a posterior (OBS-1), mild (OBS-2), and severe posterior-anterior (OBS-3) obstruction. OBS-1 and OBS-2 induced minor changes to the overall CSF pressures, while OBS-3 caused significantly larger changes with a decoupling between the intracranial and spinal compartment. Coughing led to a peak in overall CSF pressure. During this peak, pressure differences between the lateral ventricles and the spinal compartment were locally amplified for all degrees of obstruction. These results emphasize the effects of coughing and indicate that severe levels of obstruction lead to distinct changes in intracranial pressure.

Cerebrospinal fluid opening pressure values are associated with various neurologic diseases; however, numerous factors can modify this measurement. This study aims to describe factors related to modifications in opening pressure measurements in pediatric patients. Methods: A retrospective analysis of lumbar punctures in pediatric patients conducted by the neuropediatrics group with institutional standardization. Bivariate and linear regression analyses were performed to determine the association between opening pressure and variables included in the study. Results: 544 events, median age 107 months, median opening pressure 19.7 cm H2O. Bivariate analysis found no association with medication use; anesthetics that increased opening pressure were remifentanil (P = .02) and propofol (P = .05), along with a positive linear correlation between opening pressure and age (P < .0001). Multiple linear regression analysis revealed that age, BMI, male gender, and remifentanil use were associated with an increase in opening pressure, whereas corticosteroid withdrawal was associated with a reduction in opening pressure. There is an interaction between age and headache, with an association with increased opening pressure up to around 140 months. Conclusion: This study identifies factors associated with changes in opening pressure, crucial for estimating normal opening pressure values in children. Headaches, anesthetic use, and corticosteroid withdrawal are confirmed as significant factors.

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UNASSIGNED: To review the current literature related to the correlation between translaminar pressure difference (TLPD) and glaucoma.
UNASSIGNED: In this article, we conducted a literature review using MEDLINE via PubMed, Cochrane Eyes and Vision, and Google Scholar from 01/01/2010 to 31/12/2022. Search terms included \"glaucoma\", \"intraocular pressure\", \"translaminar cribrosa pressure gradient/difference\", \"intracranial pressure\", and \"cerebrospinal fluid pressure\". Of 471 results, 8 articles were selected for the meta-analysis.
UNASSIGNED: Our meta-analysis demonstrated significantly higher intraocular pressure, lower cerebrospinal fluid pressure (CSFp), and greater TLPD in high-tension and normal-tension glaucoma groups compared to healthy groups.
UNASSIGNED: The differences in CSFp and TLPD between glaucoma and healthy people detected in current studies suggests a potential relationship between TLPD and glaucoma.

BACKGROUND: Impaired cerebrospinal fluid (CSF) dynamics is involved in the pathophysiology of neurodegenerative diseases of the central nervous system and the optic nerve (ON), including Alzheimer\'s and Parkinson\'s disease, as well as frontotemporal dementia. The smallness and intricate architecture of the optic nerve subarachnoid space (ONSAS) hamper accurate measurements of CSF dynamics in this space, and effects of geometrical changes due to pathophysiological processes remain unclear. The aim of this study is to investigate CSF dynamics and its response to structural alterations of the ONSAS, from first principles, with supercomputers.
METHODS: Large-scale in-silico investigations were performed by means of computational fluid dynamics (CFD) analysis. High-order direct numerical simulations (DNS) have been carried out on ONSAS geometry at a resolution of 1.625 μm/pixel. Morphological changes on the ONSAS microstructure have been examined in relation to CSF pressure gradient (CSFPG) and wall strain rate, a quantitative proxy for mass transfer of solutes.
RESULTS: A physiological flow speed of 0.5 mm/s is achieved by imposing a hydrostatic pressure gradient of 0.37-0.67 Pa/mm across the ONSAS structure. At constant volumetric rate, the relationship between pressure gradient and CSF-accessible volume is well captured by an exponential curve. The ONSAS microstructure exhibits superior mass transfer compared to other geometrical shapes considered. An ONSAS featuring no microstructure displays a threefold smaller surface area, and a 17-fold decrease in mass transfer rate. Moreover, ONSAS trabeculae seem key players in mass transfer.
CONCLUSIONS: The present analysis suggests that a pressure drop of 0.1-0.2 mmHg over 4 cm is sufficient to steadily drive CSF through the entire subarachnoid space. Despite low hydraulic resistance, great heterogeneity in flow speeds puts certain areas of the ONSAS at risk of stagnation. Alterations of the ONSAS architecture aimed at mimicking pathological conditions highlight direct relationships between CSF volume and drainage capability. Compared to the morphological manipulations considered herein, the original ONSAS architecture seems optimized towards providing maximum mass transfer across a wide range of pressure gradients and volumetric rates, with emphasis on trabecular structures. This might shed light on pathophysiological processes leading to damage associated with insufficient CSF flow in patients with optic nerve compartment syndrome.